ライフサイエンスコーパス: cannabinoid

1 nnabinoids alone; 8% other illicit drugs +/- cannabinoids).

2 f Delta(9)-THC, and endogenous and synthetic cannabinoids.

3 ture that has examined epigenetic effects of cannabinoids.

4 ring CB1 ligands, such as THC, and synthetic cannabinoids.

5 sm underlying the psychotomimetic effects of cannabinoids.

6 activated receptors are also engaged by some cannabinoids.

7 and negative health effects of cannabis and cannabinoids.

8 ed to assess the immunomodulatory effects of cannabinoids.

9 Therapeutics aimed at blocking the cannabinoid 1 (CB1) receptor for treatment of obesity re

10 biologically active compounds targeting the cannabinoid 1 and alpha7 nicotinic acetylcholine recepto

11 The cannabinoid 1 receptor (CB1R) is one of the most abundan

12 ted with orthosteric agonists/antagonists of cannabinoid 1 receptor (CB1R), a tractable target for tr

13 of beta-arrestin-mediated signaling from the cannabinoid 1 receptor (CB1R).

14 bility of its main central molecular target, cannabinoid-1 (CB1) receptors in man.

15 Activating the renal cannabinoid-1 receptor (CB1R) induces nephropathy, where

16 ologies are also triggered by activating the cannabinoid-1 receptor (CB1R), which contributes to the

17 s in which beta-cell loss has been linked to cannabinoid-1 receptor (CB1R)-induced proinflammatory si

18 investigate the intracellular signaling from cannabinoid 2 receptor (CB2R).

19 etween enhanced production of the endogenous cannabinoid 2-arachidonoylglycerol (2-AG) and diminished

20 monstrate a critical role for the endogenous cannabinoid 2-arachidonoylglycerol (2-AG) in stress-resi

21 dy is to assess the effect of treatment with cannabinoid-2 receptor agonist HU-308 in the oral health

22 Endogenously generated cannabinoids acting via CB2 receptors play important rol

23 ctivation (JZL184, URB597) or an orthosteric cannabinoid agonist (WIN55,212-2).

24 The CB2 cannabinoid agonist LY2828360 lacked both toxicity and e

25 se (FAAH) inhibitor URB597 and the synthetic cannabinoid agonist WIN55,212-2 displayed AM251-sensitiv

26 nnabinoid deactivation and/or an orthosteric cannabinoid agonist.

27 he acute behavioral and cognitive effects of cannabinoid agonists and experience transient exacerbati

28 g evidence supporting an association between cannabinoid agonists and psychosis comes from controlled

29 d to demonstrate any "beneficial" effects of cannabinoid agonists in individuals with schizophrenia-c

30 DAT1, and AKT1) may moderate the effects of cannabinoid agonists in laboratory studies.

31 Cannabinoid agonists induce dopamine release, although t

32 rossover laboratory studies demonstrate that cannabinoid agonists, including phytocannabinoids and sy

33 action than the currently existing classical cannabinoid agonists.

34 A fourth synthetic cannabinoid, ajulemic acid (AJA; CT-3; Resunab; Corbus P

35 196) used illicit drugs during therapy (15% cannabinoids alone; 8% other illicit drugs +/- cannabino

36 Cannabinoids also modulate nociception and locomotion th

37 The two main endogenous cannabinoids, anandamide and 2-arachidonoyl glycerol (2-

38 et al. (2016) describe a novel link between cannabinoids and cognition.

39 al and clinical literature on the effects of cannabinoids and endogenous cannabinoid signaling system

40 324420) and blood, urine, and hair levels of cannabinoids and metabolites were determined.

41 on acute and chronic effects of cannabis and cannabinoids and on persistence or recovery after abstin

42 Synthetic cannabinoids and phytocannabinoids have been shown to su

43 he emerging class of "ultrapotent" synthetic cannabinoids and poses a public health concern.

44 lected natural products, e.g. capsaicinoids, cannabinoids and terpenes, by highlighting challenges an

45 tigations of the molecular mechanisms of the cannabinoids and their receptors have lacked high-resolu

46 uring treatment compared with those who used cannabinoids and/or other illicit drugs.

47 The best-studied endogenous cannabinoids are 2-arachidonoyl glycerol and arachidonoy

48 Since cannabinoids are currently in clinical use for the treat

49 As a class, the cannabinoids are generally free from the adverse effects

50 x differences in the effects of cannabis and cannabinoids are highlighted.

51 al studies show that 'medicinal' cannabis or cannabinoid-based medications relieve pain in human dise

52 rom different animal models, and develop new cannabinoid-based medicine.

53 s. non-nociceptive pathways and suggest that cannabinoid-based therapies may be more appropriate for

54 of the new compounds includes, among others, cannabinoid binding assays, functional studies, and surf

55 bolism) counteracts the rewarding effects of cannabinoids by acting as a negative allosteric modulato

56 on the sex-dependent effects of cannabis and cannabinoids by synthesizing findings from preclinical a

57 ese data suggest that both acute and chronic cannabinoids can disrupt the ability of the brain to gen

58 On July 12, 2016, a synthetic cannabinoid caused mass intoxication of 33 persons in on

59 of SCs remain biologically active, exerting cannabinoid (CB) receptor affinity, potency, and efficac

60 iosynthetic and degradative enzymes, and the cannabinoid (CB) receptors CB1 and CB2.

61 Remarkably, activation of cannabinoid (CB) receptors differentially modulated the

62 s the potential to interfere with endogenous cannabinoid (CB) regulation of fetal nervous system deve

63 ith cannabinoid receptors, predominantly the cannabinoid CB1 receptor (CB1 R) in the cerebellum; acti

64 iatum, ie, adenosine A2A receptor (A2AR) and cannabinoid CB1 receptor (CB1R), are of pivotal importan

65 Allosteric modulators of the cannabinoid CB1 receptor have recently been reported as

66 Allosteric modulators of the cannabinoid CB1 receptor were first discovered in 2005.

67 2-arachidonoylglycerol (2-AG) that activates cannabinoid CB1 receptor.

68 is believed to be mediated by activation of cannabinoid CB1 receptors (CB1Rs) on GABAergic neurons t

69 h pharmacological or genetic invalidation of cannabinoid CB1 receptors has been linked to depression

70 Drugs that act as inverse agonists of cannabinoid CB1 receptors in the brain can attenuate the

71 Activation of cannabinoid CB1 receptors suppresses pathological pain b

72 t as negative allosteric modulators (NAM) of cannabinoid CB1 receptors.

73 ng them to intravenously self-administer the cannabinoid CB1-receptor agonist WIN55,212-2.

74 ing of mice, thereby emulating the effect of cannabinoid CB1-receptor inverse agonists.

75 Type 1 cannabinoid (CB1 ) receptors are widely distributed in t

76 Endocannabinoid activation of cannabinoid (CB1) receptors known to inhibit presynaptic

77 ases 2-arachidonoylglycerol and behaves as a cannabinoid (CB1/CB2) receptor indirect agonist.

78 The cannabinoid CB2 receptor (CB2R) represents a promising t

79 Cannabinoid CB2 receptors (CB2Rs) are expressed in mouse

80 Much of the research on cannabinoids (CBs) has focused on their effects at the m

81 , and earlier age of onset) or with distinct cannabinoid compounds (i.e., THC and CBD).

82 er previously identified peripherally active cannabinoid compounds, and could have clinical applicati

83 Lower binding was negatively correlated with cannabinoid concentrations in blood and urine and was as

84 as well as the widely consumed plant (phyto)cannabinoid Delta(9)-tetrahydrocannabinol (THC)(1).

85 A method for determining cannabinoids, Delta9-tetrahidrocannabinol (THC), 11-nor-

86 rnative therapeutic approach to nicotine and cannabinoid dependence.

87 aling system in C. elegans, demonstrates the cannabinoid-dependent activation of monoaminergic signal

88 2-AG or AEA activate NPR-19 directly and cannabinoid-dependent inhibition can be rescued in npr-1

89 des a tool for the prescreening of synthetic cannabinoid derivatives in seized materials and biologic

90 Owing to the complexity of the cannabinoid-dopamine interactions that take place, there

91 his is evidenced by the ability of exogenous cannabinoid drugs to produce hedonia and maintain self-a

92 Pharmacological augmentation of endogenous cannabinoid (eCB) signaling has been suggested to repres

93 xiety is further modulated by the endogenous cannabinoid (eCB) system that attenuates the synaptic ef

94 Endogenous cannabinoids (endocannabinoids) are small molecules bios

95 comprises cannabinoid receptors, endogenous cannabinoids (endocannabinoids), and the enzymes respons

96 In these models, adolescent cannabinoid exposure has been reported to cause long-ter

97 medication) in children affected by in utero cannabinoid exposure.

98 The recovery of cannabinoids from plant material was >93%.

99 The human cannabinoid G-protein-coupled receptors (GPCRs) CB1 and

100 Given that treatment with cannabinoids has been shown to reduce invasiveness of ca

101 i-inflammatory and immunologic properties of cannabinoids have been reported in several tissues.

102 Exogenous as well as endogenous cannabinoids have been shown to target voltage-gated sod

103 For years, cannabinoids have been studied at the cellular level usi

104 The potency of the synthetic cannabinoid identified in these analyses is consistent w

105 Thus, SA of a rewarding cannabinoid in adolescence does not produce long-term co

106 I-MS method for the detection and mapping of cannabinoids in a single hair has not been reported.

107 and imaging for the detection and mapping of cannabinoids in a single hair sample.

108 hieving identification and quantification of cannabinoids in food matrices.

109 This report examines the concentration of cannabinoids in illicit cannabis products seized by the

110 However, intestinal lymphatic transport of cannabinoids in immunocompromised patients requires caut

111 This study highlights the potential role of cannabinoids in modulating monoaminergic signaling and t

112 wledge regarding the effects of cannabis and cannabinoids in PTSD and the preclinical and clinical li

113 public and research interest in the role of cannabinoids in the regulation of stress-related biologi

114 The endogenous cannabinoids, including the closely related lipoamino ac

115 resent one of the primary mechanisms whereby cannabinoids induce disruptions in attention, working me

116 uggesting that one of the mechanisms whereby cannabinoids induce psychosis is through the alteration

117 D2 antagonists allosterically modulate cannabinoid-induced CB1 coupling, signaling, and beta-ar

118 rgic system, which is critically involved in cannabinoid-induced reward.

119 Cannabinoids, inflammation, and fibrosis.

120 uces aversive effects that might explain why cannabinoid is not rewarding in rodents and might also a

121 Alleviation of neuropathic pain by cannabinoids is limited by their central nervous system

122 and feeding through a pathway requiring the cannabinoid-like receptor NPR-19.

123 Thus, several cannabinoids may be considered candidates for developmen

124 ese points, the potential mechanisms whereby cannabinoids may modulate the eCB system to ameliorate d

125 romedial medulla as an important site of the cannabinoid-mediated analgesia by acetaminophen.

126 aine, suggesting the involvement of a common cannabinoid-mediated mechanism in the cue-induced reinst

127 rmines functional properties of autapses and cannabinoid-mediated modulation of synaptic transmission

128 The synthetic cannabinoid methyl 2-(1-(4-fluorobenzyl)-1H-indazole-3-c

129 Cannabinoids modulate intestinal permeability through ca

130 in vision and present a novel mechanism for cannabinoid modulation of neuronal activity through Cl(-

131 Both THC and CBD, as well as other cannabinoid molecules, are currently being evaluated for

132 and of alpha2-adrenergic compounds, but not cannabinoid, neurotensin, or muscarinic drugs.

133 4, that involves a complex interaction among cannabinoid, octopaminergic, and serotonergic signaling.

134 itis elegans model to examine the effects of cannabinoids on behavior.

135 The mechanisms underlying the effects of cannabinoids on cognitive processes are not understood.

136 hippocampus is obligatory for the action of cannabinoids on LTP and spatial memory formation.

137 the N-acyl amino acids do not bind to either cannabinoid or opioid receptors, thus reducing adverse a

138 reases the levels of endogenous analogues of cannabinoids, or endocannabinoids.

139 Regarding cannabinoids, preclinical evidence from slice and local

140 s, including phytocannabinoids and synthetic cannabinoids, produce a wide range of positive, negative

141 potential recordings has shown that central cannabinoid receptor (cannabinoid receptor type 1) agoni

142 us, in vivo inhibition of MAGL induces a CB1 cannabinoid receptor (CB1R)-dependent suppression of inh

143 on terminals that express the primary type 1 cannabinoid receptor (CB1R); 3) binds to CB1R, which inh

144 at may enhance intravenous SA of THC and the cannabinoid receptor (CBR) agonist CP 55 940 in Old Worl

145 trate that genetic or chemical inhibition of cannabinoid receptor (Cnr) activity disrupts liver devel

146 in-2-yl)phenyl)urea (PSNCBAM-1, 2) bound the cannabinoid receptor 1 (CB1) and antagonized G protein c

147 gated the effect of treatment of mice with a cannabinoid receptor 1 (CB1) antagonist on Diet-Induced

148 The cannabinoid receptor 1 (CB1) is an inhibitory G protein-

149 The cannabinoid receptor 1 (CB1) is the principal target of

150 Cannabinoid receptor 1 (CB1) is the principal target of

151 diated by the endocannabinoid anandamide and cannabinoid receptor 1 (CB1), was significantly attenuat

152 nt on metabotropic glutamate receptor 5, and cannabinoid receptor 1 (CB1).

153 ids modulate intestinal permeability through cannabinoid receptor 1 (CB1).

154 interactor with the intracellular region of Cannabinoid Receptor 1 (CB1R, also known as Cnr1 or CB1)

155 n, but not endodermal specification: loss of cannabinoid receptor 1 (cnr1) and cnr2 activity leads to

156 ciency is not fully abrogated by the inverse cannabinoid receptor 1 agonist SR141716 (Rimonabant) sug

157 augmentation of AEA signaling and via direct cannabinoid receptor 1 stimulation with Delta(9)-tetrahy

158 t CXCR4 can form an induced heterodimer with cannabinoid receptor 2 (CB2) in human breast and prostat

159 We investigated the role of the cannabinoid receptor 2 (CB2), an important modulator of

160 we uncover a role for AEA and its receptor, cannabinoid receptor 2 (CB2), in the regulation of immun

161 t time, that transient administration of the cannabinoid receptor 2 antagonist AM630 (10 mg/kg) or in

162 ium-activated potassium (SK) channel and CB1 cannabinoid receptor activation.

163 elf-administration (SA), using the synthetic cannabinoid receptor agonist WIN55,212-2 (WIN), in order

164 esent study demonstrates that the endogenous cannabinoid receptor agonists 2-arachidonoylglycerol (2-

165 Notably, cannabinoid receptor agonists as well as inhibitors of e

166 f the acetaminophen metabolite AM 404 and of cannabinoid receptor antagonists as well as data from ti

167 Cannabinoid receptor CB2 (CB2(-/-)) mice were used as a

168 n the brain of MKO(GFAP) mice does not cause cannabinoid receptor desensitization as previously obser

169 re provides an atomic framework for studying cannabinoid receptor function, and will aid the design a

170 ve blockade or inverse agonism of the type 1 cannabinoid receptor has been tested for the improvement

171 G) and anandamide (AEA) activate a canonical cannabinoid receptor in Caenorhabditis elegans and also

172 The function of the CB2 cannabinoid receptor in the brain has long been a matter

173 The Cannabinoid Receptor Interacting Protein 1 (Cnrip1) was

174 Cannabinoid receptor interacting protein 1a (CRIP1a) is

175 he present study demonstrates that mammalian cannabinoid receptor ligands activate a conserved cannab

176 The activation of cannabinoid receptor subtype 2 (CB2R) prevents acinar ce

177 Cannabinoid receptor transmission strongly influences em

178 xiolytic, and neuroprotective efficacies via cannabinoid receptor type 1 (CB1) or type 2 (CB2) or via

179 with antagonist/inverse agonist activity at cannabinoid receptor type 1 (CB1R) and inhibitory effect

180 The cannabinoid receptor type 1 (CB1R) colocalized with TRPV

181 xpress both OX-A receptor type 1 (OX-1R) and cannabinoid receptor type 1 (CB1R) on the plasma membran

182 CRs: the alpha2A-adrenergic receptor, GABAB, cannabinoid receptor type 1 (CB1R), and dopamine recepto

183 hibitory synaptic transmission in the PL via cannabinoid receptor type 1 (CB1R)- and 2-arachidonoylgl

184 ng acute hippocampal slices, and hippocampal cannabinoid receptor type 1 and brain-derived neurotroph

185 has shown that central cannabinoid receptor (cannabinoid receptor type 1) agonists decrease the power

186 Expression of cannabinoid receptor Type 2 was reported in osteoblasts

187 Cannabinoid receptor type-1 (CB1) is known to have a sub

188 Cannabinoid receptor type-1 (CB1) plays a crucial role i

189 t subpopulation of NAc FSIs that express the cannabinoid receptor type-1 (CB1).

190 lucose-feedback sensor) and CNR2 (encoding a cannabinoid receptor) as central effectors of B-lymphoid

191 19-null animals by the expression of a human cannabinoid receptor, CB1, highlighting the orthology of

192 itron emission tomography scan each with the cannabinoid receptor-1 (CB1R) selective radiotracer [(11

193 perties by virtue of its ability to activate cannabinoid receptor-2 (CB-2) expressed on immune cells.

194 nflammatory IL-10 cytokines, in part through cannabinoid receptor-2 activation.

195 nyl)ethyl amide (WOBE437) exerted pronounced cannabinoid receptor-dependent anxiolytic, antiinflammat

196 tein, and the inactivation of DAGLs disrupts cannabinoid receptor-dependent synaptic plasticity and i

197 s of regular cannabis users, particularly in cannabinoid receptor-high areas, which are vulnerable to

198 uced A-type potassium current (IA) through a cannabinoid receptor-independent mechanism mimicked by a

199 By discussing the mechanisms of cannabinoid receptor-mediated signaling events at critic

200 PR55 has been postulated to serve as a novel cannabinoid receptor.

201 bitory effects demonstrated by activation of cannabinoid receptors (CB) on cancer proliferation and m

202 s on type 1 orexin receptors (OX1Rs), type 1 cannabinoid receptors (CB1Rs) and diacylglycerol lipase

203 Type 1 cannabinoid receptors (CB1Rs) are widely expressed in th

204 We investigated in mice the role of CB1 cannabinoid receptors (CB1Rs) in memory impairment and s

205 s unknown, as is the potential modulation by cannabinoid receptors (CBRs).

206 ions emerged across regions that are high in cannabinoid receptors (i.e., hippocampus, prefrontal cor

207 The endocannabinoid system comprises cannabinoid receptors 1 and 2 (CB1 and CB2), their endog

208 NADA is also an agonist of cannabinoid receptors 1 and 2.

209 gnaling system, comprising G protein-coupled cannabinoid receptors and their endogenous lipid-derived

210 The most abundant cannabinoid receptors are the CB1 cannabinoid receptors;

211 The cannabinoid receptors have been the targets of intensive

212 Cannabinoid receptors in the BLA contribute to anxiogene

213 Notably, cannabinoid receptors serve as molecular targets for the

214 Cannabinoid receptors type 2 (CB2) represent a target wi

215 The ECS comprises cannabinoid receptors, endogenous cannabinoids (endocann

216 associated metabolic enzymes, together with cannabinoid receptors, predominantly the cannabinoid CB1

217 th unforeseen opposite allosteric effects on cannabinoid receptors, suggests its potential role in pe

218 the CB1 cannabinoid receptors; however, CB2 cannabinoid receptors, transient receptor potential chan

219 Potential therapeutic targets include the cannabinoid receptors, type 1 and 2, as well as biosynth

220 ts of 2-AG are mediated by G-protein-coupled cannabinoid receptors.

221 gement of the enteric nervous system through cannabinoid receptors.

222 es of these SCs retain their activity at the cannabinoid receptors.

223 them (14b) being selective versus classical cannabinoid receptors.

224 rostaglandin synthesis than by activation of cannabinoid receptors.

225 olites of these SCs retain their activity at cannabinoid receptors.

226 ical effects through their interactions with cannabinoid receptors.

227 nists (21) is fully selective versus classic cannabinoid receptors.

228 y arachidonic acid, which has no activity on cannabinoid receptors.

229 e periphery and interact with peripheral CB2 cannabinoid receptors.

230 be high affinity ligands for the CB1 and CB2 cannabinoid receptors.

231 t abundant cannabinoid receptors are the CB1 cannabinoid receptors; however, CB2 cannabinoid receptor

232 The levels of cannabinoids recovered in the intestinal lymphatic syste

233 As the effects of KYNA on cannabinoid reward involve nicotinic receptors, in the p

234 e chromenopyrazole ring, a versatile CB1/CB2 cannabinoid scaffold.

235 Synthetic cannabinoids (SCs) are the largest group of compounds cu

236 Synthetic cannabinoids (SCs) continue to be the largest group of n

237 ught to develop a rodent model of adolescent cannabinoid self-administration (SA), using the syntheti

238 ystem of the brain and subsequently increase cannabinoid self-administration in adulthood-suggest a m

239 In the fetal nervous system, (endo)cannabinoid-sensing receptors and the enzymatic machiner

240 Functional assays in mouse show cannabinoid sensitivity changes and Cnrip1 has recently

241 Although cannabinoids show therapeutic promise in other areas, ro

242 es emotional processing, and disturbances in cannabinoid signaling are associated with various neurop

243 g, and highlights the advantages of studying cannabinoid signaling in a genetically tractable whole-a

244 gic signaling and the advantages of studying cannabinoid signaling in a genetically tractable, whole-

245 demonstrate a critical role for hippocampal cannabinoid signaling in the modulation of mesolimbic ne

246 Our present data indicate that enhanced cannabinoid signaling is also responsible for the analge

247 mechanism by which striatal cholinergic and cannabinoid signaling leads to sustained reductions in d

248 theless, the mechanisms by which intra-vHipp cannabinoid signaling may modulate mesolimbic activity s

249 binoid receptor ligands activate a conserved cannabinoid signaling system in C. elegans and also modu

250 This study defines a conserved cannabinoid signaling system in C. elegans, demonstrates

251 n the effects of cannabinoids and endogenous cannabinoid signaling systems in the regulation of biolo

252 tion, including a facilitation of endogenous cannabinoid signaling via one of its metabolites.

253 To better understand cannabinoid signaling, we have used the Caenorhabditis e

254 Recent work also demonstrates deficient cannabinoid signalling in the mouse 'ducky(2J) ' model o

255 Exogenous cannabinoids, such as tetrahydrocannabinol, produce thei

256 to harness the therapeutic potential of the cannabinoid system and other GPCRs.

257 the data illustrate a mechanism by which the cannabinoid system can negatively modulate CXCR4 recepto

258 Our results indicate that the cannabinoid system contributes not only to acetaminophen

259 Investigations of the endogenous cannabinoid system in the prefrontal cortex of subjects

260 and will aid the design and optimization of cannabinoid system modulators for therapeutic ends.

261 The natural cannabinoid system of the brain is complex and involved

262 However, the contribution of the cannabinoid system to antihyperalgesia against inflammat

263 rbances in the development of the endogenous cannabinoid system, are discussed.

264 -/-) mice, confirming the involvement of the cannabinoid system.

265 by receptors that are part of an endogenous cannabinoid system.

266 expression, cell toxicity, induction of the cannabinoid tetrad, depressive- and anxiety-like behavio

267 tly less variety and lower concentrations of cannabinoids than are observed in state-legal U.S. dispe

268 ceptible to the immunosuppressive effects of cannabinoids than those from healthy volunteers or cance

269 Anandamide (AEA) is an endogenous intestinal cannabinoid that controls appetite and energy balance by

270 In contrast, cannabinoids that are beta-arrestin-biased--such as THC

271 ic transcriptional and behavioral effects of cannabinoids that have been observed within one's lifeti

272 Given that the endogenous cannabinoid (that is, endocannabinoid) system modulates

273 search showed that in situ derivatization of cannabinoids through addition of an N-methylpyridium gro

274 tudy, we further investigated the ability of cannabinoids to modulate sodium currents from wild-type

275 gs, drugs for neuropathic pain, opioids, and cannabinoids, to physical therapy strategies and prevent

276 chidonoylglycerol (2-AG), via stimulation of cannabinoid type 1 (CB1) receptor and Ca(2+)/calmodulin-

277 The cannabinoid type 1 (CB1) receptor and the capsaicin rece

278 nnabinol (THC), CBD does not act through the cannabinoid type 1 (CB1) receptor but has many other rec

279 Deletion of cannabinoid type 1 (CB1) receptors from cortical project

280 reliably causes a downregulation or loss of cannabinoid type 1 (CB1) receptors.

281 he metabotropic glutamate 5 receptor and the cannabinoid type 1 receptor are G protein-coupled recept

282 tatory response upon activation, whereas the cannabinoid type 1 receptor, mainly present at presynapt

283 Analysis of individual connections revealed cannabinoid type 1 receptor-mediated suppression of the

284 ays in rats, we tested whether activation of cannabinoid type 1 receptors (CB1R) in the vHipp may mod

285 rectly activate TRPV1 and inhibit it through cannabinoid type 1 receptors (CB1Rs) and cAMP pathways.

286 erentiated adipocytes is blocked by AM251, a cannabinoid type 1 receptors antagonist.

287 one of these peptides, DITADDEPLT activates cannabinoid type 1 receptors.

288 slightly better inverse agonist activity at cannabinoid type 1 receptors.

289 ndocannabinoid system, and in particular the cannabinoid type 2 receptor (CB2R), raised the interest

290 mic, hippocampal, and peripheral blockade of cannabinoid type-1 (CB1) receptors abolished the stress-

291 projection neurons, we investigated whether cannabinoid type-1 receptor (CB1R) activation is necessa

292 Here we show that cannabinoid type-1 receptors (CB1Rs) control hippocampal

293 long been recognized as potent and selective cannabinoid type-2 receptor (CB2R) ligands.

294 al effects are mostly due to the presence of cannabinoids, unique natural products, whose pharmacolog

295 We show that the engagement of the cannabinoid/vanilloid receptors augments the number and

296 In this study, six cannabinoids were tested for signaling bias in in vitro

297 are involved in the tetrad assay induced by cannabinoids which had been associated with CB1R agonism

298 Therefore, administering cannabinoids with a high-fat meal or in lipid-based form

299 In pursuit of safer controlled-deactivation cannabinoids with high potency and short duration of act

300 Here we show that oral co-administration of cannabinoids with lipids can substantially increase thei